It has been hypothesized that chronic consumption of ethanol leads to hepatic hypermetabolism. The hypermetabolic state is thought to result in regional hypoxia and consequent central lobular necrosis in the liver of chronic alcoholics. Although careful studies have indicated that many of the data originally reported could not be reproduced, it remains possible that thyroid action on the liver is modified after long-term ethanol ingestion by attenuating the action of T-3. Previous work has indicated that extracts of bovine pituitaries have the capacity to lower the response of whole-animal minimal oxygen consumption (MOC) to thyroid hormones. By using primary cultures of rat hepatocytes, it has been possible to show that one active ingredient of the pituitary extracts is growth hormone (GH). GH lowers the response of hepatocyte malic enzyme (ME) and glycerol-3-phosphate dehydrogenase (G-3-PDH) and fatty acid synthase (FAS) activities to T-3, insulin, dexamethasone, and glucose after 6 days in culture. Since episodic secretion of GH has been reported to be blunted by ethanol, altered secretion patterns of GH in rats chronically treated with ethanol may account for the elevated activity of G-3-PDH in the absence of changes in circulating levels of thyroid hormones.